ORIGINAL RESEARCH article
Front. Cardiovasc. Med.
Sec. Cardiovascular Pharmacology and Drug Discovery
This article is part of the Research TopicTherapeutic Targeting of Cell Death in Cardiovascular Diseases: From Mechanisms to Clinical ApplicationsView all 6 articles
THR-123, A NOVEL BMP-7 MIMETIC THAT ACTIVATES AKT PHOSPHORYLATION AND INHIBITS CARDIOMYOCYTE APOPTOSIS AND INFLAMMATION, PROTECTS HEART FROM MYOCARDIAL INJURY (MI) IN RAT MODEL
Provisionally accepted
William Carlson1,2,3*
Romesh Subramanian1,2,3
Dattatreyamurty Bosukonda1,2,3
Philippe Bey1
Peter C. Keck1
Frederic Roy Carlson, Jr.1- 1MassGeneraHospital-Harvard Medical School, Boston, United States
- 2Harvard Medical School, Boston, United States
- 3Massachusetts General Hospital, Boston, United States
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Acute myocardial infarction continues to be the most common cause of heart failure despite the advancements in the treatment of MI over the past 20 years. We have developed "BMP mimetics" that selectively activate the BMP signaling pathway, and do not induce bone formation. A BMP-7 mimetic, THR-123, is anti-inflammatory, anti-apoptotic, anti-fibrotic and promotes tissue regeneration. In an animal model of ischemia-reperfusion using LAD coronary occlusion-induced myocardial injury, THR-123 markedly decreased myocardial infarct size (84%) and pericardial inflammation. The mechanism of action of THR-123 was examined in three different cellular (cardiomyocytes) models. Mechanistically, THR-123 activates Akt phosphorylation and inhibits inflammation and apoptosis in cardiomyocytes. These results show that the BMP-7 mimetic (THR-123) protects cardiomyocytes, and limits infarct size after myocardial ischemia and reperfusion injury. THR-123 may provide a novel pharmacological intervention in myocardial injury.
Keywords: animal model, BMP mimetic, Ischemia-Reperfusion (I/R) injury, Myocardial Infarction, THR-123
Received: 20 Oct 2025; Accepted: 16 Feb 2026.
Copyright: © 2026 Carlson, Subramanian, Bosukonda, Bey, Keck and Carlson, Jr.. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: William Carlson
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